The pathophysiology and treatment of postischemic hypoperfusion after complete cerebral ischemia

本实验采用犬短暂性全脑缺血模型，研究了无复流现象和缺血后延迟性低灌注（PDH）对脑功能恢复的影响。阻断升主动脉建立心房转流，造成脑缺血，无复流：100 mmHg压力阻断升、降主动脉，经主动脉弓注入胶体碳100-200 ml。通过测量脑冠状面胶体碳染色面积计算无复流率。缺血15 min后观察无复流现象的形成。主动脉阻断后立即用生理盐水稀释脑血，导致无复流面积减少。再循环开始后3分钟，稀释组为冠状动脉断面表面的10%，而对照组超过70%。5分钟后，两组均小于10%。稀释组在24-48 h脑功能恢复较好。PDH：缺血15分钟后，在缺血后反应性充血后6-10小时，观察到大脑皮层和脑干中的血流量减少20-40%。尼卡地平1 μ g/kg/min的给药纠正了PDH，导致脑功能的改善。结论：我们证实，15分钟的完全脑缺血引起的无复流现象和PDH，这两个都有助于脑功能的恶化，并治疗它们导致缺血后脑功能的改善。

We studied the influences of no-reflow phenomenon and postischemic delayed hypoperfusion (PDH) on recovery of brain functions after transient complete cerebral ischemia using dogs. Cerebral ischemia was produced by clamping of ascending aorta with aorto-atrial bypass formation.No-reflow phenomenon: 100-200 ml of colloidal carbon was injected through aortic arch with 100 mmHg-pressure clamping ascending and descending aorta. The ratio of no-reflow was calculated by measuring the area of colloidal carbon staining on surfaces of coronary section of brain. The formation of no-reflow phenomenon was observed after 15 min of ischemia. Dilution of blood of the brain by physiological saline immediately after aortic clamping resulted in decrease in the no-reflow area. Three min after start of recirculation it was 10% of the surface of coronary section in the dilution group, but more than 70% in the control. After 5 min it was less than 10% in both groups. The brain functions were better in dilution group after 24-48 h. The efficacy of dilution was demonstrated also in histological examination of hippocampal CAl pyramidal cells.PDH: After 15 min of ischemia 20-40% decrease in blood flow in both cerebral cortex and brain stem was observed for 6-10 h following postischemic reactive hyperemia. The administration of Nicardipine 1 ug/kg/min corrected the PDH resulting in improvement of brain functions.Conclusion: We confirmed that 15 min of complete cerebral ischemia brings about both no-reflow phenomenon and PDH, that both contribute deterioration of brain functions, and that treatment of them results in the improvement of postischemic brain functions.